On the Ca2+-permeability of neurons and glia.
Fractions enriched in pinched-off nerve terminals and astrocytic glial cells were used to analyse the permeability of Ca++ of the two membranes. Three experimental models were used to illustrate a principle difference of the excitatory versus the no-excitatory cell membrane, with respect to Ca-permeability. The effect of an increased [Ca++] on 86Rb+ and 3H-GABA transport was measured in medium containing low and high [K+]. The possibility of GABA stimulation of release of preaccumulated 45Ca+4 with low and high [K+] was compared in neurons and glia. Finally, the effect of depolarizing [K+] on the transmembranal Ca++-gradient was measured by comparing the efficacy of the Ca-ionophore A23187 to depolarize or to inhibit the 3H-GABA uptake at these different [K+]. The data essentially confirms the picture of a potential dependent Ca++-permeability in the neuron, while the permeability of the glial cells seems a "true" constant. It might be relevant to suggest the astrocyte a role as a "Ca-buffer" with possibilities to control extracellular Ca+4 in cases of hyperactivity, this in analogy with what has been suggested for K+.
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002463:Cell Membrane Permeability / Q000187:drug effects; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012413:Rubidium / Q000378:metabolism; D013574:Synaptosomes / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000001:Calcimycin; D005680:gamma-Aminobutyric Acid; D012413:Rubidium; D011188:Potassium; D002118:Calcium